Diabetes increases the risk of heart failure approximately 2.5-fold, independent of coronary artery disease and other comorbidities. This process, termed diabetic cardiomyopathy, is characterized by initial impairment of left ventricular (LV) relaxation followed by LV contractile dysfunction. Post-mortem examination reveals that human diastolic dysfunction is closely associated with LV damage, including cardiomyocyte hypertrophy, apoptosis and fibrosis, with impaired coronary microvascular perfusion. The pathophysiological mechanisms underpinning the characteristic features of diabetic cardiomyopathy remain poorly understood, although multiple factors including altered lipid metabolism, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum (ER) stress, inflammation, as well as epigenetic changes, are implicated. Despite a recent rise in research interrogating these mechanisms and an increased understanding of the clinical importance of diabetic cardiomyopathy, there remains a lack of specific treatment strategies. How the chronic metabolic disturbances observed in diabetes lead to structural and functional changes remains a pertinent question, and it is hoped that recent advances, particularly in the area of epigenetics, among others, may provide some answers. This review hence explores the temporal onset of the pathological features of diabetic cardiomyopathy, and their relative contribution to the resultant disease phenotype, as well as both current and potential therapeutic options. The emergence of glucose-optimizing agents, namely glucagon-like peptide-1 (GLP-1) agonists and sodium/glucose co-transporter (SGLT)2 inhibitors that confer benefits on cardiovascular outcomes, together with novel experimental approaches, highlight a new and exciting era in diabetes research, which is likely to result in major clinical impact.
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May 2017
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Image demonstrates the ultrastructural cortical basement membrane changes in SHRSP brain: accumulation of lipofuscin in pericytes. For further details, see article by Screiber et al in this issue (pages 1001–1013). Image kindly provided by Stefanie Schreiber.
Review Article|
May 04 2017
Are targeted therapies for diabetic cardiomyopathy on the horizon?
Mitchel Tate;
Mitchel Tate
1Heart Failure Pharmacology, Baker Heart & Diabetes Institute, Melbourne, Vic 3004, Australia
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David J. Grieve;
David J. Grieve
2Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast BT9 5HN, U.K.
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Rebecca H. Ritchie
1Heart Failure Pharmacology, Baker Heart & Diabetes Institute, Melbourne, Vic 3004, Australia
3Department of Medicine (Central Clinical School), Monash University, Melbourne, Vic 3004, Australia
Correspondence: Rebecca Ritchie ([email protected])
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Publisher: Portland Press Ltd
Received:
December 07 2016
Revision Received:
February 02 2017
Accepted:
February 03 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (10): 897–915.
Article history
Received:
December 07 2016
Revision Received:
February 02 2017
Accepted:
February 03 2017
Citation
Mitchel Tate, David J. Grieve, Rebecca H. Ritchie; Are targeted therapies for diabetic cardiomyopathy on the horizon?. Clin Sci (Lond) 1 May 2017; 131 (10): 897–915. doi: https://doi.org/10.1042/CS20160491
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